Recently, we and others have demonstrated that in vivo GITR ligation using an agonist anti-GITR mAb, DTA-1, can augment anti-tumor T-cell responses and induce tumor rejection in B16 melanoma and other murine models.[14], [15], [16], [17], [18], [19] However, the mechanism(s) by which GITR ligation leads to tumor rejection remain unclear. The gene discussed is TNFRSF18; the disease is melanoma.